The mortality and morbidity from ischemic heart disease results primarily from atheromatous narrowings of the coronary arteries. Although various medical and surgical therapies may improve the quality of lifestyle of most patients with symptomatic coronary atherosclerosis, these therapies do not favorably change the underlying anatomy responsible for the coronary luminal narrowings and therefore do not prevent the occurrence of future cardiac events such as occurrence of worsening of signs and symptoms of myocardial ischemia, myocardial infarction and sudden death.
Percutaneous transluminal coronary angioplasty (PTCA) has recently been developed as an alternative method of treatment of coronary atherosclerosis. During cardiac catheritization an inflatable balloon is inserted in a coronary artery at the region of a coronary narrowing. Inflation of the balloon for 15-60 seconds results in expansion of the narrowed lumen or passageway. Because residual narrowing is usually present after the first balloon inflation, multiple inflations are routinely performed in an attempt to reduce the severity of the residual stenosis or tube narrowing. Despite these multiple inflations, a mild to moderately severe residual stenosis usually is present after successful PTCA.
One of the major problems with such treatment is that a flap of material occasionally is formed during the treatment which, after withdrawal of the instrumentation, falls back into theartery causing abrupt reclosure. This necessitates emergency coronary artery bypass surgery and thus PTCA is potentially dangerous and often provides only a temporary treatment of symptoms of obstructive coronary arterial atherosclerosis. The reason that the flap is formed is that upon balloon inflation the surrounding material is broken or fragmented which causes blood to enter the arterial wall between planes of dissection. This causes the arterial wall to swell acutely and either reduces the size of the channel or completely obliterates the channel resulting in a five percent incidence of abrupt reclosure.
Moreover with present PTCA procedures, postmortem pathologic studies show that disruption of the arterial wall and atheromatous plaque occurs following balloon inflation, including fracture of the plaque and separation of tissue layers, e.g., dissection. Angiographically a shaggy or hazy appearance of the coronary lumen is often seen and evidence for overt dissection is often apparent following successful PTCA. Disruption of the arterial wall temporarily increases the size of the coronary channel but predisposes to deposition of platelets and microthrombi which very likely contribute to the greater than 25% incidence of restenosis within three to six months following successful PTCA.
By way of further background, recent studies have been reported using lasers to perform vascular anastomoses so that end-to-end and end-to-side arterial and vein grafting can be achieved without sutures. The basic principle simply involves placing the free edges of a vessel and the graft in close proximity and heating these tissues with either an argon-ion, neodymium:YAG, or CO.sub.2 laser. Cross linking of collagen and other tissue proteins occurs and a coagulation is observed pathologically following the treatment. The tissue integrity is maintained, however, and the tensile strength of the "sutureless" anastomosis rivals that of anastomoses performed with sutures used in a conventional manner. Moreover, short and long term tissue healing appears to be better with the laser thermal fusion of tissues than with the suture technique.